Acute peritonitis-induced adipose CD127ILC1s express PD-L1 and ameliorate inflammation in mice.

Abstract

Peritonitis is an inflammation of the peritoneum primarily caused by gut perforation and consequent bacterial leakage, a known cause of sepsis. Although adipose tissue is recognized as an immunologically active organ, the involvement of adipose tissue innate lymphoid cells (ILC) in regulating peritonitis remains poorly understood. Here, we employ a cecal ligation and puncture mouse model and demonstrate that circulating CD127group 1 ILC (ILC1) migrate into the mesenteric adipose tissue (MAT) during the inflammatory period of peritonitis. CD127ILC1s undergo phenotypic changes to become CD127ILC1s, resulting in an increased number of CD127ILC1s in the MAT. We also show that this population of CD127ILC1s expresses PD-L1, exhibits low IFN-γ production, and potentially acts as a negative regulator of TNF production by γδ T cells, thereby controlling acute peritonitis. Our findings suggest that MAT-CD127ILC1s play an important regulatory role in acute peritonitis and may represent a potential therapeutic target for sepsis.